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Your search keyword '"Koschmieder, Steffen"' showing total 19 results
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19 results on '"Koschmieder, Steffen"'

3. ROP-ET: a prospective phase III trial investigating the efficacy and safety of ropeginterferon alfa-2b in essential thrombocythemia patients with limited treatment options

Author

Kiladjian, Jean-Jacques, Marin, Francisca Ferrer, Al-Ali, Haifa Kathrin, Alvarez-Larrán, Alberto, Beggiato, Eloise, Bieniaszewska, Maria, Breccia, Massimo, Buxhofer-Ausch, Veronika, Cerna, Olga, Crisan, Ana-Manuela, Danaila, Catalin Doru, De Stefano, Valerio, Döhner, Konstanze, Empson, Victoria, Gora-Tybor, Joanna, Griesshammer, Martin, Grosicki, Sebastian, Guglielmelli, Paola, García-Gutierrez, Valentin, Heidel, Florian H., Illés, Arpád, Tomuleasa, Ciprian, James, Chloe, Koschmieder, Steffen, Krauth, Maria-Theresa, Krejcy, Kurt, Lazaroiu, Mihaela-Cornelia, Mayer, Jiri, Nagy, Zsolt György, Nicolini, Franck-Emmanuel, Palandri, Francesca, Pappa, Vassiliki, Reiter, Andreas Johannes, Sacha, Tomasz, Schlager, Stefanie, Schmidt, Stefan, Terpos, Evangelos, Unger, Martin, Wölfler, Albert, Cirici, Blanca Xicoy, and Klade, Christoph

Published
2024
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5. Proinflammatory phenotype of iPS cell-derived JAK2 V617F megakaryocytes induces fibrosis in 3D in vitro bone marrow niche

Author

Flosdorf, Niclas, Böhnke, Janik, de Toledo, Marcelo A.S., Lutterbach, Niklas, Lerma, Vanesa Gómez, Graßhoff, Martin, Olschok, Kathrin, Gupta, Siddharth, Tharmapalan, Vithurithra, Schmitz, Susanne, Götz, Katrin, Schüler, Herdit M., Maurer, Angela, Sontag, Stephanie, Küstermann, Caroline, Seré, Kristin, Wagner, Wolfgang, Costa, Ivan G., Brümmendorf, Tim H., Koschmieder, Steffen, Chatain, Nicolas, Castilho, Miguel, Schneider, Rebekka K., and Zenke, Martin

Published
2024
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6. Non-canonical Hedgehog signaling mediates profibrotic hematopoiesis-stroma crosstalk in myeloproliferative neoplasms

Author

Pritchard, Jessica E., Pearce, Juliette E., Snoeren, Inge A.M., Fuchs, Stijn N.R., Götz, Katrin, Peisker, Fabian, Wagner, Silke, Benabid, Adam, Lutterbach, Niklas, Klöker, Vanessa, Nagai, James S., Hannani, Monica T., Galyga, Anna K., Sistemich, Ellen, Banjanin, Bella, Flosdorf, Niclas, Bindels, Eric, Olschok, Kathrin, Biaesch, Katharina, Chatain, Nicolas, Bhagwat, Neha, Dunbar, Andrew, Sarkis, Rita, Naveiras, Olaia, Berres, Marie-Luise, Koschmieder, Steffen, Levine, Ross L., Costa, Ivan G., Gleitz, Hélène F.E., Kramann, Rafael, and Schneider, Rebekka K.

Published
2024
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7. Indication and management of allogeneic haematopoietic stem-cell transplantation in myelofibrosis: updated recommendations by the EBMT/ELN International Working Group

Author

Kröger, Nicolaus, Bacigalupo, Andrea, Barbui, Tiziano, Ditschkowski, Markus, Gagelmann, Nico, Griesshammer, Martin, Gupta, Vikas, Hamad, Nada, Harrison, Claire, Hernandez-Boluda, Juan Carlos, Koschmieder, Steffen, Jain, Tania, Mascarenhas, John, Mesa, Ruben, Popat, Uday R, Passamonti, Francesco, Polverelli, Nicola, Rambaldi, Alessandro, Robin, Marie, Salit, Rachel B, Schroeder, Thomas, Scott, Bart L, Tamari, Roni, Tefferi, Ayalew, Vannucchi, Alessandro M, McLornan, Donal P, and Barosi, Giovanni

Published
2024
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8. NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms

Author

Koerber, Ruth-Miriam, primary, Krollmann, Calvin, additional, Cieslak, Kevin, additional, Tregel, Elisabeth, additional, Brümmendorf, Tim H., additional, Koschmieder, Steffen, additional, Griesshammer, Martin, additional, Gütgemann, Ines, additional, Brossart, Peter, additional, Skoda, Radek C., additional, Kolbe, Carl Christian, additional, Latz, Eicke, additional, Wolf, Dominik, additional, and Teichmann, Lino L., additional

Published
2024
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11. Activating mutations in JAK2 and CALR differentially affect intracellular calcium flux in store operated calcium entry.

Author

Bhuria, Vikas, Franz, Tobias, Baldauf, Conny, Böttcher, Martin, Chatain, Nicolas, Koschmieder, Steffen, Brümmendorf, Tim H., Mougiakakos, Dimitrios, Schraven, Burkhart, Kahlfuß, Sascha, and Fischer, Thomas

Subjects
INTRACELLULAR calcium, ERYTHROPOIETIN receptors, CALCIUM, PHYSIOLOGIC salines, CELL physiology, CELL migration, CELL growth
Abstract

Background: Calcium (Ca2+) signaling regulates various vital cellular functions, including integrin activation and cell migration. Store-operated calcium entry (SOCE) via calcium release-activated calcium (CRAC) channels represents a major pathway for Ca2+ influx from the extracellular space in multiple cell types. The impact of JAK2-V617F and CALR mutations which are disease initiating in myeloproliferative neoplasms (MPN) on SOCE, calcium flux from the endoplasmic reticulum (ER) to the cytosol, and related key signaling pathways in the presence or absence of erythropoietin (EPO) or thrombopoietin (TPO) is poorly understood. Thus, this study aimed to elucidate the effects of these mutations on the aforementioned calcium dynamics, in cellular models of MPN. Methods: Intracellular Ca2+ levels were measured over a time frame of 0–1080 s in Fura-2 AM labeled myeloid progenitor 32D cells expressing various mutations (JAK2-WT/EpoR, JAK2-V617F/EpoR; CALR-WT/MPL, CALR-ins5/MPL, and del52/MPL). Basal Ca2+ concentrations were assessed from 0–108 s. Subsequently, cells were stimulated with EPO/TPO in Ca2+-free Ringer solution, measuring Ca2+ levels from 109–594 s (store depletion). Then, 2 mM of Ca2+ buffer resembling physiological concentrations was added to induce SOCE, and Ca2+ levels were measured from 595–1080 s. Fura-2 AM emission ratios (F340/380) were used to quantify the integrated Ca2+ signal. Statistical significance was assessed by unpaired Student's t-test or Mann–Whitney-U-test, one-way or two-way ANOVA followed by Tukey's multiple comparison test. Results: Following EPO stimulation, the area under the curve (AUC) representing SOCE significantly increased in 32D-JAK2-V617F cells compared to JAK2-WT cells. In TPO-stimulated CALR cells, we observed elevated Ca2+ levels during store depletion and SOCE in CALR-WT cells compared to CALR-ins5 and del52 cells. Notably, upon stimulation, key components of the Ca2+ signaling pathways, including PLCγ-1 and IP3R, were differentially affected in these cell lines. Hyper-activated PLCγ-1 and IP3R were observed in JAK2-V617F but not in CALR mutated cells. Inhibition of calcium regulatory mechanisms suppressed cellular growth and induced apoptosis in JAK2-V617F cells. Conclusions: This report highlights the impact of JAK2 and CALR mutations on Ca2+ flux (store depletion and SOCE) in response to stimulation with EPO and TPO. The study shows that the JAK2-V617F mutation strongly alters the regulatory mechanism of EpoR/JAK2-dependent intracellular calcium balance, affecting baseline calcium levels, EPO-induced calcium entry, and PLCγ-1 signaling pathways. Our results reveal an important role of calcium flux in the homeostasis of JAK2-V617F positive cells. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Targeting Endothelial-to-Mesenchymal Transition in a 3D iPSC-Based Model of JAK2V617F+ Myeloproliferative Neoplasms

Author

Caduc, Madeline J., Baqueró Lopez, Cristina, Grasshoff, Martin, Miriam Buhl, Eva, Elsafi Mabrouk, Mohamed H., Ernst, Sabrina, Wong, Dickson W.L., Müller-Newen, Gerhard, Vogt, Michael, Eschweiler, Jörg, Boor, Peter, Ackermann, Maximilian, Franzen, Julia, Costa, Ivan G., Zenke, Martin, Brümmendorf, Tim H., Koschmieder, Steffen, and Szymanski de Toledo, Marcelo

Published
2024
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15. MPN-179 Targeting Endothelial-to-Mesenchymal Transition in a 3D iPSC-Based Model of JAK2V617F+ Myeloproliferative Neoplasms

Author

Caduc, Madeline J., Cristinaó Lopez, Cristina, Grasshoff, Martin, Miriam Buhl, Eva, Elsafi Mabrouk, Mohamed H., Ernst, Sabrina, Dickson. L. Wong, Dickson, Gerhardüller-Newen, Gerhard, Vogt, Michael, Eschweiler, Jörg, Boor, Peter, Ackermann, Maximilian, Franzen, Julia, Costa, Ivan G., Zenke, Martin, Brümmendorf, Tim H., Koschmieder, Steffen, and de Toledo, Marcelo Szymanski

Published
2024
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17. Proposals for Revised International Working Group-European LeukemiaNet Criteria for Anemia Response in Myelofibrosis

Author

Tefferi, Ayalew, Barosi, Giovanni, Passamonti, Francesco, Hernandez-Boluda, Juan-Carlos, Bose, Prithviraj, Döhner, Konstanze, Ellis, Martin, Gangat, Naseema, Garcia, Jacqueline S., Gisslinger, Heinz, Gotlib, Jason, Guglielmelli, Paola, Gupta, Vikas, Harrison, Claire, Hexner, Elizabeth O., Hobbs, Gabriela S., Kiladjian, Jean-Jacques, Koschmieder, Steffen, Kroger, Nicolaus, Kuykendall, Andrew T., Loscocco, Giuseppe G., Mascarenhas, John, Masarova, Lucia, Mesa, Ruben, Mora, Barbara, Odenike, Olatoyosi, Oh, Stephen T., Pardanani, Animesh, Patel, Anand, Pemmaraju, Naveen, Rambaldi, Alessandro, Rampal, Raajit, Sirhan, Shireen, Szuber, Natasha, Talpaz, Moshe, Vachhani, Pankit J., Vannucchi, Alessandro M., and Barbui., Tiziano

Abstract

1.An international panel of 38 experts and clinical trialists in myelofibrosis participated in the preparation of the current document.2.New definitions of transfusion status, gender-specific hemoglobin thresholds, and criteria for major and minor responses are submitted.

Published
2024
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18. Antithrombotic Therapy in Cancer Patients with Cardiovascular Diseases: Daily Practice Recommendations by the Hemostasis Working Party of the German Society of Hematology and Medical Oncology (DGHO) and the Society for Thrombosis and Hemostasis Research (GTH e.V.)

Author

Parmentier, Stefani, Koschmieder, Steffen, Henze, Larissa, Griesshammer, Martin, Matzdorff, Axel, Bakchoul, Tamam, Langer, Florian, Alesci, Rosa Sonja, Duerschmied, Daniel, Thomalla, Goetz, and Riess, Hanno

Published
2024
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19. Oncogenic Calreticulin Induces Immune Escape by Stimulating TGF-β Expression and Regulatory T Cell Expansion in the Bone Marrow Microenvironment.

Author

Schmidt D, Endres C, Hoefflin R, Andrieux G, Zwick M, Karantzelis N, Staehle HF, Vinnakota JM, Duquesne S, Mozaffari Jovein M, Pfeifer D, Becker H, Blazar BR, Zähringer A, Duyster J, Brummer T, Boerries M, Baumeister J, Shoumariyeh K, Li J, Green AR, Heidel FH, Tirosh I, Pahl HL, Leimkühler N, Köhler N, de Toledo MAS, Koschmieder S, and Zeiser R

Abstract

Increasing evidence supports the interplay between oncogenic mutations and immune escape mechanisms. Strategies to counteract the immune escape mediated by oncogenic signaling could provide improved therapeutic options for patients with various malignancies. As mutant calreticulin (CALR) is a common driver of myeloproliferative neoplasms (MPN), we analyzed the impact of oncogenic CALRdel52 on the bone marrow (BM) microenvironment in MPN. Single-cell RNA-sequencing revealed that CALRdel52 led to the expansion of TGF-β1-producing erythroid progenitor cells and promoted the expansion of FoxP3+ regulatory T cells (Treg) in a murine MPN model. Treatment with an anti-TGF-β antibody improved mouse survival and increased the glycolytic activity in CD4+ and CD8+ T cells in vivo, while T cell depletion abrogated the protective effects conferred by neutralizing TGF-β. TGF-β1 reduced perforin and TNF-α production by T cells in vitro. TGF-β1 production by CALRdel52 cells was dependent on JAK1/2, PI3K, and ERK activity, which activated the transcription factor Sp1 to induce TGF-β1 expression. In four independent patient cohorts, TGF-β1 expression was increased in the BM of MPN patients compared to healthy individuals, and the BM of MPN patients contained a higher frequency of Treg compared to healthy individuals. Together, this study identified an ERK/Sp1/TGF-β1 axis in CALRdel52 MPNs as a mechanism of immunosuppression that can be targeted to elicit T-cell-mediated cytotoxicity.

Published
2024
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